Neurology Research Center, Helen Hayes Hospital, West Haverstraw, New York 10993-1195, USA, and Departments of Pharmacology and Neurology, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA
Limbic seizures have often been attributed to pathology in the
hippocampus, such as the well described condition termed Ammon's
Horn sclerosis, in which many of the hippocampal principal cells
have degenerated. However, several studies in both the clinical
and basic literature indicate that the parahippocampal region
may also play an important role. This region sustains a characteristic
pattern of damage in most animal models of epilepsy that is
similar to that identified in humans with intractable temporal
lobe epilepsy. Perhaps the most striking aspect of parahippocampal
pathology is the marked loss of neurons in layer III of the
entorhinal cortex. The similarity of cell loss in layer III
and cell loss in the hilus of the dentate gyrus is compared,
as is the characteristic resistance of layer II neurons and
dentate granule cells. Cellular electrophysiological results
are used as a basis for the hypothesis that synaptic inhibition
plays a role in the relative vulnerability of these neurons.
Studies of neurogenesis in both areas is also discussed. It
is proposed that this may be an additional factor that influences
vulnerability in these areas.
